The role of the subependymal plate in the origin of gliomas induced by ethylnitrosourea in the rat brain

1977 ◽  
Vol 33 (4) ◽  
pp. 521-522 ◽  
Author(s):  
P. L. Lantos
Keyword(s):  
Rat Brain ◽  
Subependymal Plate

Role of Glutathione monoester on age‐related neurochemical alterations in rat brain

2009 ◽  
Vol 27 (7) ◽  
pp. 643-648
Author(s):  
Ganesan Murali ◽  
Sugumar Dhivya ◽  
Periannan Rasappan
Keyword(s):  
Rat Brain ◽  
Age Related

scholarly journals The role of Ca2+ in the protoveratrine-induced release of γ-aminobutyrate from rat brain slices

1980 ◽  
Vol 190 (2) ◽  
pp. 333-339 ◽  
Author(s):  
M C W Minchin
Keyword(s):  
Cerebral Cortex ◽  
Rat Brain ◽  
Dose Response ◽  
Transmitter Release ◽  
Response Curve ◽  
Brain Slices ◽  
Veratrum Alkaloids ◽  
Similar Dose ◽  
22Na Uptake

1. Protoveratrine A increased the release of gamma-amino[3H]butyrate from small slices of rat cerebral cortex. This effect increased with increasing protoveratrine concentration, reaching a maximum at 100 microM. 2. Removal of Ca2+ from the superfusing medium did not change the increase in release due to 10 microM-protoveratrine; however, the Ca2+ antagonists, compound D-600, La3+, Mn2+, Mg2+ and also high Ca2+ concentration inhibited the effect of the alkaloid, as did procaine. 3. Protoveratrine A increased the uptake of 22Na+ into the slices with a similar dose-response curve to that found for gamma-aminobutyrate release. For the most part, the substances that inhibited protoveratrine-stimulated gamma-aminobutyrate release also inhibited 22Na+ uptake, although the correlation was not perfect. 4. Although extracellular Ca2+ is not required for protoveratrine-induced gamma-aminobutyrate release, an increase in Na+ influx that is susceptible to inhibition by some Ca2+ antagonists does appear to be associated with this phenomenon. However, the possibility remains that changes in the free intracellular Ca2+ concentration may be important for transmitter release induced by depolarizing veratrum alkaloids.

Protective Role of Gallic Acid on Sodium Fluoride Induced Oxidative Stress in Rat Brain

2012 ◽  
Vol 89 (1) ◽  
pp. 73-77 ◽  
Author(s):  
Seyed Fazel Nabavi ◽  
Solomon Habtemariam ◽  
Mahtab Jafari ◽  
Antoni Sureda ◽  
Seyed Mohammad Nabavi
Keyword(s):  
Oxidative Stress ◽  
Rat Brain ◽  
Gallic Acid ◽  
Sodium Fluoride ◽  
Protective Role

Effect of neonatal hypothyroidism on maturation of nuclear triiodothyronine (T3) receptors in developing rat brain

1980 ◽  
Vol 95 (4) ◽  
pp. 495-499 ◽  
Author(s):  
Kazumasa Ishiguro ◽  
Yukichi Suzuki ◽  
Tamotu Sato
Keyword(s):  
Rat Brain ◽  
Binding Capacity ◽  
Physiological Role ◽  
Brain Maturation ◽  
Control Group ◽  
High Concentration ◽  
Neonatal Hypothyroidism ◽  
Developing Rat ◽  
T3 Receptors

Abstract. Changes of nuclear T3 receptors during brain maturation were studied in normal and hypothyroid rats. In normal rats, the higher receptor concentration present in the neonatal period (0.35 ± 0.04 ng T3/mg DNA) decreased at the age of 14 days (0.25 ± 0.02 ng T3/mg DNA), and remained at this level thereafter to 35 days of age (0.25 ± 0.03 T3/mg DNA). In contrast, hypothyroid rats showed a significantly higher concentration than that found in an age-matched control group at the age of 14 days (0.38 ± 0.07 ng T3/mg DNA), and maintained this level up to 35 days of age (0.37 ± 0.03 T3/mg DNA). The binding affinity was similar in both groups and throughout maturation (mean ± sd in normal groups: 1.9 ± 0.3 × 1010m−1, in hypothyroid groups: 1.7 ± 0.2 × 1010m−1). Plasma T3 concentrations showed changes reciprocal to those in the binding capacity of T3 receptors. These results indicate that nuclear T3 receptors in rat brain mature by the age of 14 days, in association with a decrease in binding capacity, and this process seems to be T3-dependent. The physiological role of the high concentration of T3 receptors observed in neonatal and hypothyroid rat brain during development is at present not clear.

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